Effects of nitric oxide synthase blockade on esophageal peristalsis and the lower esophageal sphincter in the cat.

The present study explores the role of nitric oxide (NO) in control of esophageal peristalsis and lower esophageal sphincter (LES) function in the cat. Studies were performed on 20 ketamine-anesthetized cats with manometric recording at the LES, 0, 2, 4, and 6 cm above the LES (smooth muscle section), and 12 and (or) 14 cm above the LES (striated muscle section). L-Ng-Nitro-arginine (L-NNA, 10(-6)-10(-4) mol/kg) was given intravenously, and the effects on swallow-induced esophageal peristalsis were assessed. (i) L-NNA increased the velocity of swallow-induced peristalsis in the smooth muscle esophagus; the effect was dose dependent, more prominent distally, and completely reversed by L-arginine (10(-3) mol/kg). (ii) L-NNA decreased the amplitude of peristaltic contraction in the very distal esophagus; the decrease also was dose dependent but not returned to normal by L-arginine. (iii) L-NNA inhibited LES relaxation (reversed by L-arginine) and decreased the LES "after-contraction" amplitude (unaffected by L-arginine). (iv) L-NNA was associated with the appearance of repetitive contractions. Basal LES tone was unaffected by L-NNA. In conclusion, NO is an important mediator for the timing of peristalsis in the distal smooth muscle esophagus and for LES relaxation in the cat, a species whose contraction amplitude is largely determined by cholinergic excitation. The role of NO in controlling esophageal body and LES contraction amplitude, and in preventing repetitive contractions, requires further study.